The Society for the Study of Reproduction 41st Annual Meeting, Kailua-Kona, HI, 27-30 May 2008, Abstract no. 608 How to Cite?

Abstract

Toll-Like Receptors (TLRs) are the main family of pathogen pattern
recognition receptors and constitute a major part of the innate immune
system. Reports from our laboratory and others have demonstrated the
existence of TLRs in the human female reproductive tract. However, little
has been done to identify TLRs function in the female reproductive tract,
particularly in the fallopian tubes. Sex hormones can influence TLRs
expression in the female reproductive tract. However, it is not known if
sex hormones can influence TLRs function in the fallopian tubes. The aim
of the current investigation was to test the existence of TLR3 in an
immortalised human fallopian tube epithelial cell line (OE-E6/E7) and to
test the effect of sex hormones on the function of TLR3 in this cell line.
TLR3 protein was detected by immunostaining in OE-E6/E7. RT-PCR was
also used to show the existence of TLR3 gene in OE-E6/E7. To study the
function of TLR3 in OE-E6/E7 cells, these cells were exposed to TLR3
specific ligand (poly I:C) and the levels of IL-1 and IL-6 released were
measured in OE-E6/E7 culture media using ELISA. The effect of sex
hormones on the function of TLR3 in OE-E6/E7 cells was investigated by
treating these cells with poly I:C (25 microgram/ml for 24 hours) in the
presence of different concentrations of estradiol and progesterone. Cells
were divided into following groups; control (without any additional
treatment of sex hormones), E1 (1nM/ml estradiol), E10 (10nM/ml
estradiol), E1000 (1000nM/ml estradiol), P1 (1nM/ml progesterone),
P10(10nM/ml progesterone), P100 (100nM/ml progesterone) and P1000
(1000nM/ml progesterone) respectively. Both immunohistochemistry and
RT-PCR verified the existence of TLR3 in OE-E6/E7 cells. These cells did
not produce any detectable amount of IL-1 in the presence or absence of
TLR3 ligand. However, the production of IL-6 was significantly increased
in the presence of poly (I:C). Although both sex hormones had a
suppressive and biphasic effect on the production of IL-6 in the presence
and absence of poly (I:C), when the ratio level of responses between
control and test groups to Poly (I:C) in the presence of different
concentrations of sex hormones was calculated, it was apparent that the
presence of increasing levels of sex hormones enhanced TLR3 response to
its specific ligand (poly (I:C)) in OE-E6/E7 cells. It seems sex hormones
regulate the function of TLRs in the female reproductive tract during
different stages of the female reproductive/menstrual cycle.

Toll-Like Receptors (TLRs) are the main family of pathogen pattern
recognition receptors and constitute a major part of the innate immune
system. Reports from our laboratory and others have demonstrated the
existence of TLRs in the human female reproductive tract. However, little
has been done to identify TLRs function in the female reproductive tract,
particularly in the fallopian tubes. Sex hormones can influence TLRs
expression in the female reproductive tract. However, it is not known if
sex hormones can influence TLRs function in the fallopian tubes. The aim
of the current investigation was to test the existence of TLR3 in an
immortalised human fallopian tube epithelial cell line (OE-E6/E7) and to
test the effect of sex hormones on the function of TLR3 in this cell line.
TLR3 protein was detected by immunostaining in OE-E6/E7. RT-PCR was
also used to show the existence of TLR3 gene in OE-E6/E7. To study the
function of TLR3 in OE-E6/E7 cells, these cells were exposed to TLR3
specific ligand (poly I:C) and the levels of IL-1 and IL-6 released were
measured in OE-E6/E7 culture media using ELISA. The effect of sex
hormones on the function of TLR3 in OE-E6/E7 cells was investigated by
treating these cells with poly I:C (25 microgram/ml for 24 hours) in the
presence of different concentrations of estradiol and progesterone. Cells
were divided into following groups; control (without any additional
treatment of sex hormones), E1 (1nM/ml estradiol), E10 (10nM/ml
estradiol), E1000 (1000nM/ml estradiol), P1 (1nM/ml progesterone),
P10(10nM/ml progesterone), P100 (100nM/ml progesterone) and P1000
(1000nM/ml progesterone) respectively. Both immunohistochemistry and
RT-PCR verified the existence of TLR3 in OE-E6/E7 cells. These cells did
not produce any detectable amount of IL-1 in the presence or absence of
TLR3 ligand. However, the production of IL-6 was significantly increased
in the presence of poly (I:C). Although both sex hormones had a
suppressive and biphasic effect on the production of IL-6 in the presence
and absence of poly (I:C), when the ratio level of responses between
control and test groups to Poly (I:C) in the presence of different
concentrations of sex hormones was calculated, it was apparent that the
presence of increasing levels of sex hormones enhanced TLR3 response to
its specific ligand (poly (I:C)) in OE-E6/E7 cells. It seems sex hormones
regulate the function of TLRs in the female reproductive tract during
different stages of the female reproductive/menstrual cycle.